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1 Department of Molecular and Cellular Physiology, and 2 Department of Surgery, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130
Two strains of endothelial nitric oxide
synthase (eNOS)-deficient (
/) mice have been developed that respond
differently to myocardial ischemia-reperfusion (MI/R). We
evaluated both strains of eNOS
/ mice in an in vivo
model of MI/R. Harvard (Har) eNOS/ mice
(n = 12) experienced an 84% increase in myocardial
necrosis compared with wild-type controls (P < 0.05).
University of North Carolina (UNC) eNOS/
(n = 10) exhibited a 52% reduction in myocardial
injury versus wild-type controls (P < 0.05). PCR
analysis of myocardial inducible NO synthase (iNOS) mRNA levels
revealed a significant (P < 0.05) increase in the UNC
eNOS/ mice compared with wild-type mice, and there was
no significant difference between the Har eNOS/ and
wild-type mice. UNC eNOS/ mice treated with an iNOS
inhibitor (1400W) exacerbated the extent of myocardial necrosis. When
treated with 1400W, Har eNOS/ did not exhibit a
significant increase in myocardial necrosis. These data demonstrate
that two distinct strains of eNOS/ mice display
opposite responses to MI/R. Although the protection seen in the UNC
eNOS/ mouse may result from compensatory increases in
iNOS, other genes may be involved.
heart; infarct; ischemia-reperfusion
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